Ganong's Review of Medical Physiology, 23rd Edition

476
SECTION V
Gastrointestinal Physiology

The movements of the colon include segmentation contrac-
tions and peristaltic waves like those occurring in the small
intestine. Segmentation contractions mix the contents of the
colon and, by exposing more of the contents to the mucosa,
facilitate absorption. Peristaltic waves propel the contents
toward the rectum, although weak antiperistalsis is some-
times seen. A third type of contraction that occurs only in the
colon is the
mass action contraction,
in which there is simul-
taneous contraction of the smooth muscle over large conflu-
ent areas. These contractions move material from one portion
of the colon to another (Clinical Box 28–4). They also move
material into the rectum, and rectal distention initiates the
defecation reflex (see below).
The movements of the colon are coordinated by the BER of
the colon. The frequency of this wave, unlike the wave in the
small intestine, increases along the colon, from about 2/min at
the ileocecal valve to 6/min at the sigmoid.

TRANSIT TIME IN THE SMALL

INTESTINE & COLON

The first part of a test meal reaches the cecum in about 4 h, and
all the undigested portions have entered the colon in 8 or 9 h.
On average, the first remnants of the meal traverse the first
third of the colon in 6 h, the second third in 9 h, and reach the
terminal part of the colon (the sigmoid colon) in 12 h. From
the sigmoid colon to the anus, transport is much slower (Clin-
ical Box 28–5). When small colored beads are fed with a meal,
an average of 70% of them are recovered in the stool in 72 h,
but total recovery requires more than a week. Transit time,
pressure fluctuations, and changes in pH in the gastrointesti-
nal tract can be observed by monitoring the progress of a small
pill that contains sensors and a miniature radio transmitter.

DEFECATION

Distention of the rectum with feces initiates reflex contrac-

tions of its musculature and the desire to defecate. In humans,

the sympathetic nerve supply to the internal (involuntary)

anal sphincter is excitatory, whereas the parasympathetic sup-

ply is inhibitory. This sphincter relaxes when the rectum is

distended. The nerve supply to the external anal sphincter, a

skeletal muscle, comes from the pudendal nerve. The sphinc-

ter is maintained in a state of tonic contraction, and moderate

distention of the rectum increases the force of its contraction

(Figure 28–8). The urge to defecate first occurs when rectal

pressure increases to about 18 mm Hg. When this pressure

reaches 55 mm Hg, the external as well as the internal sphinc-

ter relaxes and there is reflex expulsion of the contents of the

rectum. This is why reflex evacuation of the rectum can occur

even in the setting of spinal injury.

Before the pressure that relaxes the external anal sphincter

is reached, voluntary defecation can be initiated by straining.

Normally, the angle between the anus and the rectum is

approximately 90 degrees (Figure 28–9), and this plus con-

traction of the puborectalis muscle inhibit defecation. With

straining, the abdominal muscles contract, the pelvic floor is

lowered 1 to 3 cm, and the puborectalis muscle relaxes. The

anorectal angle is reduced to 15 degrees or less. This is com-

bined with relaxation of the external anal sphincter and

FIGURE 28–7
The human colon.

Ascending

colon

Descending

colon

Ileum

Tenia

coli

Haustra

Sigmoid colon

Internal

External

anal

sphincter

Rectum

Appendix

Cecum

Hepatic flexure

Transverse colon

Splenic flexure

CLINICAL BOX 28–4

Hirschsprung Disease

Some children present with a genetically determined con-

dition of abnormal colonic motility known as Hirschsprung

disease or

aganglionic megacolon,

which is characterized

by abdominal distention, anorexia, and lassitude. The dis-

ease is typically diagnosed in infancy, and affects as many

as 1 in 5000 live births. It is due to a congenital absence of

the ganglion cells in both the myenteric and submucous

plexuses of a segment of the distal colon, as a result of fail-

ure of the normal cranial-to-caudal migration of neural

crest cells during development. The action of endothelins

on the endothelin B receptor (see Chapter 7) are necessary

for normal migration of certain neural crest cells, and

knockout mice lacking endothelin B receptors developed

megacolon. In addition, one cause of congenital agangli-

onic megacolon in humans appears to be a mutation in the

endothelin B receptor gene. The absence of peristalsis in

patients with this disorder causes feces to pass the agangli-

onic region with difficulty, and children with the disease

may defecate as infrequently as once every 3 wk. The

symptoms can be relieved completely if the aganglionic

portion of the colon is resected and the portion of the

colon above it anastomosed to the rectum.